Do we eat too much salt—or not? More from the 2014 Consensus Conference on Nutrition

We all eat too much salt, right? And even if we’re perfectly healthy right now, without individual and population-level efforts to reduce our sodium intake, we are all placing ourselves at risk of the ensuing adverse health consequences. Aren’t we? The depth of the debate on this issue was on full display, from some of its leading protagonists, at last week’s Consensus Conference on Nutrition. While I have tended towards cynicism about this debate, considering the influence of the salt industry lobby, what mildly surprised me—and I suspect may surprise many health professionals and most of the public—was how rational and soundly based the arguments are on both sides, and how hard it actually is for an evidence-based clinician to reconcile the two.

The average Canadian consumes 3400 mg of salt per day. This is well above the level recommended in most guidelines. Health Canada’s recommendation has long been that Canadians should aim to consume 1500 mg or less per day and should not exceed 2300 mg per day. However, in 2013 the Canadian Hypertension Education Program (CHEP) stirred controversy when it increased the sodium intake limit recommended in its latest guidelines to 2000 mg per day. This may have been grounded partly in pragmatism, considering the feasibility of getting Canadians to consume lower amounts, but it also brought CHEP’s recommendations in line with those from the World Health Organization’s 2012 evidence-based review. Mary L'Abbé, Professor and Chair of of Nutritional Sciences at the University of Toronto and a member of the WHO nutritional guidelines subgroup on diet and health, reviewed the process of developing this guideline and its findings. Based on a systematic review of randomized trials and prospective cohort studies, reducing sodium intake was found to be associated with a modest reduction in blood pressure, but of a magnitude deemed clinically significant. No clear effect was found on cardiovascular disease overall, but reducing sodium appears to reduce the specific risks of stroke and fatal coronary disease, albeit based on low quality evidence.

The U.S. Institute of Medicine issued a report in 2013 reviewing the evidence for the benefits and harms of different levels of dietary sodium for preventing cardiovascular disease. Jamy Ard, Associate Professor of Epidemiology and Prevention at Wake Forest School of Medicine and member of the Institute of Medicine Committee on the Consequences of Sodium Reduction in Populations, described the report and its major findings. Bottom line: the population should decrease excessive sodium intake, based on good evidence for its association with cardiovascular disease, particularly stroke. However, the report was unable to assert a clear definition of what excessive intake is, concluding only that evidence is insufficient that lowering sodium intake below 2300 mg per day affects cardiovascular disease outcomes.

The definition of “excessive” intake is of course the crux of the whole debate. It is generally agreed that the more one reduces sodium intake, the lower blood pressure will be in proportion, but the experts in the room highlighted the substantial controversy over how well such blood pressure reductions would translate into reductions in cardiovascular events, or at least whether they translate to similar risk reductions in all individuals. Conference chair Salim Yusuf highlighted some limitations of the meta-analyses on which the WHO and IOM reports were based. One salient issue is ecological fallacy, in that the presence and severity of hypertension substantially influences the effect of reducing sodium intake on blood pressure, while normal persons without hypertension or pre-hypertension display little or no blood pressure reduction with decreased sodium intake. On this basis, some question whether reducing salt intake would confer any benefits to normal healthy individuals. We do not give antihypertensive medications to healthy people with normal blood pressures as a primary prevention strategy—is the intervention of reducing salt intake really any different in nature? Even in hypertension, assumptions about health benefits from blood pressure reductions are at odds with randomized trials that have shown no benefits of lowering systolic blood pressure below 140 mmHg with medications in otherwise healthy people. Also, effects on subgroups examined in meta-analyses are subject to reporting bias, in that studies only contribute to these analyses if they chose to report on the subgroups in question. Dr. Yusuf highlighted the need for a meta-analysis that would pool individual patient data from past studies in order to provide clearer evidence.

Disagreements over what a "normal" level of sodium intake is deepen when physiological evidence is considered in addition to evidence-based nutrition. Data from experimental animals supports adverse effects of prolonged increased salt intake on the heart, blood vessels and kidneys. It seems to me, however, that drawing conclusions from this for human health depends on how accurately such models can represent normal human dietary intake patterns. According to Theodore Kotchen, Professor in the Division of Endocrinology, Metabolism, and Clinical Nutrition at the Medical College of Wisconsin, a key difference between hypertensive and normotensive persons is in renal sensitivity to salt: hypertension is associated with a "natriuretic handicap", in that a higher renal perfusion pressure is required to excrete a given amount of sodium. This salt sensitivity has been shown to be modified by genetics and race (in particular, hypertension in African Americans occurs in the presence of a lower plasma renin activity and higher aldosterone levels compared to hypertension in other racial groups). Sodium retention resulting from this renal sensitivity may then signal neural and vascular mechanisms that further potentiate sodium retention. Of note, salt sensitivity is also modified by potassium intake, which on a population level is to low; increasing our dietary potassium intake to match our sodium intake is another dietary strategy that can address this problem, as the WHO also recommends.

David McCarron, Visiting Professor of Nutrition at the University of California-Davis, expanded on the physiological basis for estimating normal sodium intake, observing that our drive to consume sodium is mediated by neurological signals that come from aldosterone and angiotensin II, thus indicating that sodium consumption is a physiologically set parameter. As further evidence for this, our taste receptors for salt are unique in having bidirectional effects: when they detect lower levels of salt, they stimulate appetite, but at higher levels, they stimulate aversion to further consumption. What I find missing from this argument, however, is the fact that our taste preferences for sodium have been shown to be modifiable based on our consumption habits: after a few weeks, persons who reduce their sodium intake adjust to the lower level, no longer perceive foods to lack salt, and may begin to perceive foods they previously consumed as too salty. This would seem to suggest that our physiological set point for sodium may be modifiable by behavioural and environmental factors, which would seem to have crucial implications for the process of estimating what normal intake is.

Another estimate of what our body considers normal sodium intake can be obtained from looking at the point at which homeostatic mechanisms kick in to cause the body to retain sodium: this is represented by plasma renin activity, which in healthy individuals begins to increase from basal levels when sodium intake drops below an average of 2300 mg per day—equivalent to the consumption level recommended by US guidelines. Interestingly, this also approximates the lower limit of how much sodium populations in different regions of the world will consume if left to their own devices. Dr. McCarron, who has been a controversial leading figure in the salt debate for his contrarian views as well as his consulting relationship with the salt industry, emphasized how the sodium intake varies across place and time within a relatively narrow range from about 2300 mg to 5000 mg per day, despite vast differences in dietary habits and changes in the composition of available foods. According to him, this argues against the sodium content of the food supply being the driver of our sodium intake, and instead supports the notion that humans are physiologically driven to adjust their consumption in response to dietary availability.

In refutation to these arguments, Lawrence Appel, Professor of Epidemiology and International Health at Johns Hopkins University, presented the case for population-wide sodium reduction based on the near-ubiquity of hypertension risk (which approaches 90% over a lifetime), its high population prevalence (a quarter of all adults in the world have hypertension) and its leading contribution to the global burden of disease. Blood pressure rises throughout life, but the rate of rise is associated with sodium intake. There is evidence that this process begins in childhood, perhaps even in infancy. While acknowledging the physiological phenomenon of sodium sensitivity, Dr. Appel pointed out that there is no readily available test for this at present. People should therefore not assume that concerns about sodium intake don't apply to them unless and until they develop hypertension; rather, these concerns probably apply to almost everyone.

Another area of great controversy is whether a low sodium intake might actually be harmful. Some studies have documented increased cardiovascular events with lower levels of sodium intake, while other large studies have not. Niels Graudal, Senior Consultant in the Department of Rheumatology at Copenhagen University Hospital, presented results from his recently published systematic review that compared studies of low v. usual or usual v. high sodium intake. Low sodium was associated with increased all-cause mortality. Martin O'Donnell, Associate Clinical Professor of Hematology and Thromboembolism at McMaster University, presented soon to be published results from the large Prospective Urban Rural Epidemiological (PURE) cohort study, which has observed a similar J-shaped association with sodium intake and mortality. Dr. Appel questioned whether this association was true, suggesting that more likely explanations are reverse causality (sick patients reducing their food intake overall) or measurement error (underreporting of sodium intake being associated with poorer health behaviors). However, Dr. O'Donnell observed that persons with low sodium intake in these studies are precisely those who are meeting current guidelines for dietary sodium. "It is illogical to say that participants with the lowest measured sodium had implausible levels of intake—and yet recommend that intake level for the whole population," he stated.

Citing further concerns about low sodium intake, Dr. McCarron pointed to evidence that hyponatremia, even at low levels, is associated with increased mortality. I questioned him as to whether introducing such evidence into the debate over dietary salt in healthy populations is disingenuous. He conceded that physiological evidence is lacking that dietary restriction alone could induce hyponatremia in healthy individuals, and that patients with hyponatremia typically have relevant medical comorbidities and are on sodium-depleting medications such as diuretics. However, he raised the thoughtful point that such patients represent a large subset of the population and are often put in situations where they cannot control their dietary intake, such as when confined to hospital, live-in chronic care facilities, or require caregiver support in their homes. Perhaps the potential for the debate over recommended sodium consumption in healthy populations to have unintended consequences on those with chronic medical conditions does bear further thought and scrutiny.

In the face of all the above conflicting evidence and methodological limitations of studies to date, many of the experts called for—you guessed it—more research. “The presence of uncertainty calls for defining the uncertainty, not for a population-wide experiment” asserted Dr. MaCarron. However, Dr. Appel pointed out that conducting a randomized trial of dietary sodium reduction costs an estimated $25,000 per patient enrolled. So it would seem that compelling evidence that could forge consensus on this issue will not be arriving any time soon. There was one thing that everyone at the conference agreed on: eating too much salt is bad for your health. If only we could figure out just how much is too much.